There are a number of theoretical debates about aging. One is the question of whether we are "programmed to die". Those who believe this think that at a point creatures get to a stage where the organism at a cellular level starts processes which deliberately set out to end the life of the multicellular organism. Another potentially contradictory view is simply that creatures accumulate damage up the point at which they can no longer survive.
It is possible, however, to look at different species and see how their lifespan operates. What is clear is that different species age in different ways. Some species don't age in the same way as others. It is worth having a look at how species vary and to what extent that explains the relationship between evolution and lifespan.
Firstly, it is clear that there are species where the adult commits some form of suicide after mating. Octopuses and Pacific Salmon
There are, however, also species which have negligible senescence. For example Bechstein's Bats, Naked Mole Rats and Bigmouth Buffalo Fish
Hive Creatures (eg NMR) such as Bees and Ants have distinctive phenotypes for the Queen.
However, the BBF and BB are creatures where the population is limited by external circumstances. In terms of BBF it is the predation of the young and BB it is environmental catastrophies.
A particularly interesting species is Hydra oligactis. This species lives in two different ways depending on the temperature. At 22 degrees centigrade it replicates by asexual budding, but if you cool it to 10 degrees it starts replicating sexually, but also aging and then dying after 60 days.
What I think is clear from the above is that evolution can and does select both to extend normal lifespan and to reduce it.
Edit 12/2/15
Peter Lidsky did a post on twitter on 11/2/15
Here he adds another different variation evolutionary pressures on lifespan with the Carnivorous Marsupials. This is where the creature dies after procreating to avoid being infected by an infectious cancer.
I think his underlying argument here is probably correct although I don't think this is the only or even main reason for evolution setting a lifespan in the interests of species fitness more generally. It, however, fits with this post so I have added this. On the other hand I disagree with his conclusion that dealing with molecular damage will not resolve it - when this relates to damage to mtDNA, of course.
Thinking practically if grandparents compete for resources with their grandchildren then the species is likely to run out of resources. I think this is probably normally a stronger pressure for limiting lifespans.
We then have the question as to what the role of aging is in terms of development. My own personal view is that aging is simply a continuation of the development process using the cytosolic acetyl-CoA levels to determine mRNA splicing and gene expression options. However, there is a broader view which is similar called hyperfunction.
There is then the cellular reprogramming camp who believe that there is somewhere that we have not yet found that there is a backup copy of the development program which can be reset. (I think this is wrong as I think the development programme is primarily driven by metabolism and we know where all the molecules are).
There is also a programmed theory of aging in that at a point creatures robustly set out to die. That can be seen in the Pacific Salmon (above) and Octopuses, but I don't think that is true about most mammals.
On the other hand I do think that our average lifespan is programmed by our genes and other things we inherit life from (such as the cellular membrane). Our genes establish the balance between damage to mitochondrial DNA and repair of that DNA. This dynamic equilibrium affects how quickly we age and as consequence our average lifespan. I accept that it would be reasonable to say there that this is a form of programming. However, I do not myself describe it as "programmed aging" in the sense that applies to Pacific Salmon and Octopuses.
I wrote about recent mtDNA research here.
Edit: 8/3/25
Aging as a mitochondria-mediated atavistic program: can aging be switched off?
Is a paper I recently saw although it was published in 2005. In this paper it says:
As was noticed by Wallace and Weismann, some of organisms of this kind are constructed in a way predetermining death shortly after reproduction. For instance, imagos of mayflies die within a few days since they cannot eat due to lack of functional mouth and their intestines are filled with air.2 In the mite Adactilidium, the young hatch inside the mother’s body and eat their way out.50 The male of some squids dies just after transferring his spermatophore to a female.51 The female octopus stops eating when her children are hatched. This does not occur if her optical glands are removed. Such an operation results in a four-fold increase in life span of the animal.52 Bamboo can live for 15–20 years reproducing vegetatively but then, in the year of flowering, dies at the height of the summer time immediately after the ripening of the seeds (see Skulachev8 for discussion). Striking observations were made in studies of salmon. The Pacific salmon was shown to die immediately after spawning as a result of accelerated aging (progeria), which develops when the fish leaves the ocean and swims along a river to its upper reaches. The traditional explanation of this kind of death was that the animal spends too much energy when swimming in the river for a long distance against current. However, this point of view proved to be wrong since (1) aging and death did not occur if gonads or adrenal glands were removed53 and (2) progeria was observed even when the river was very short and current was weak. In the Far East of Russia, two populations of salmon were compared, one spawning in the upper reaches of the Amur river (thousands of kilometers long) and another spawning in a very small river on the Sakhalin island (only 0.2 km long). In both cases, the spawning fish showed typical traits of aging that resulted in death. A signal for progeria proved to be change from the sea to fresh water. In this example, a biological function of suicide seems to be that the remains of the old fish become food for river invertebrates who, in turn, are food for the young fish.54
The Atlantic salmon, in contrast to its Pacific relative, after spawning in a river returns from river to ocean. If it is the summer generation of the fish, it often dies in the fall. A Russian ichthyologist V.V. Ziuganov has recently studied larvae of a mollusk (pearl mussel Margaritifera margaritifera) that develops in gills of the Atlantic salmon. He found that larvae can somehow switch off the fish’s “death program” so the larvae-infected fish live at least one season more than the majority of non-infected salmon (some of infected salmon live up to 13 years). An increase in the host’s life span is needed for the larvae to complete their own development. It was shown that the infected fish had fewer tumors and were more resistant to wounds and burns.54 Leng and colleagues55 reported that a peptide from another mollusk related to the mussel, a Mercenaria meretrix, activates superoxide dismutase but inhibits tyrosinase and proliferation of carcinoma cells. Earlier it was shown that a Mercenaria extract possesses anticancer activity and decreases the blood sugar and fat.55
It is possible, however, to look at different species and see how their lifespan operates. What is clear is that different species age in different ways. Some species don't age in the same way as others. It is worth having a look at how species vary and to what extent that explains the relationship between evolution and lifespan.
Firstly, it is clear that there are species where the adult commits some form of suicide after mating. Octopuses and Pacific Salmon
There are, however, also species which have negligible senescence. For example Bechstein's Bats, Naked Mole Rats and Bigmouth Buffalo Fish
Hive Creatures (eg NMR) such as Bees and Ants have distinctive phenotypes for the Queen.
However, the BBF and BB are creatures where the population is limited by external circumstances. In terms of BBF it is the predation of the young and BB it is environmental catastrophies.
A particularly interesting species is Hydra oligactis. This species lives in two different ways depending on the temperature. At 22 degrees centigrade it replicates by asexual budding, but if you cool it to 10 degrees it starts replicating sexually, but also aging and then dying after 60 days.
What I think is clear from the above is that evolution can and does select both to extend normal lifespan and to reduce it.
Edit 12/2/15
Peter Lidsky did a post on twitter on 11/2/15
I am happy to announce the winner of last Friday's Aging Puzzle!
— Peter Lidsky (@LidskyPeter) February 12, 2025
Congratulations to @tpr720 and Tasmanian devil!
(Only Tim will get his signed paperback, we don't ship books to devils).
The answer to the question about the evolutionary determinant of semelparity in carnivorous… pic.twitter.com/cnJAuP9TMr
Here he adds another different variation evolutionary pressures on lifespan with the Carnivorous Marsupials. This is where the creature dies after procreating to avoid being infected by an infectious cancer.
I think his underlying argument here is probably correct although I don't think this is the only or even main reason for evolution setting a lifespan in the interests of species fitness more generally. It, however, fits with this post so I have added this. On the other hand I disagree with his conclusion that dealing with molecular damage will not resolve it - when this relates to damage to mtDNA, of course.
Thinking practically if grandparents compete for resources with their grandchildren then the species is likely to run out of resources. I think this is probably normally a stronger pressure for limiting lifespans.
We then have the question as to what the role of aging is in terms of development. My own personal view is that aging is simply a continuation of the development process using the cytosolic acetyl-CoA levels to determine mRNA splicing and gene expression options. However, there is a broader view which is similar called hyperfunction.
There is then the cellular reprogramming camp who believe that there is somewhere that we have not yet found that there is a backup copy of the development program which can be reset. (I think this is wrong as I think the development programme is primarily driven by metabolism and we know where all the molecules are).
There is also a programmed theory of aging in that at a point creatures robustly set out to die. That can be seen in the Pacific Salmon (above) and Octopuses, but I don't think that is true about most mammals.
On the other hand I do think that our average lifespan is programmed by our genes and other things we inherit life from (such as the cellular membrane). Our genes establish the balance between damage to mitochondrial DNA and repair of that DNA. This dynamic equilibrium affects how quickly we age and as consequence our average lifespan. I accept that it would be reasonable to say there that this is a form of programming. However, I do not myself describe it as "programmed aging" in the sense that applies to Pacific Salmon and Octopuses.
I wrote about recent mtDNA research here.
Edit: 8/3/25
Aging as a mitochondria-mediated atavistic program: can aging be switched off?
Is a paper I recently saw although it was published in 2005. In this paper it says:
As was noticed by Wallace and Weismann, some of organisms of this kind are constructed in a way predetermining death shortly after reproduction. For instance, imagos of mayflies die within a few days since they cannot eat due to lack of functional mouth and their intestines are filled with air.2 In the mite Adactilidium, the young hatch inside the mother’s body and eat their way out.50 The male of some squids dies just after transferring his spermatophore to a female.51 The female octopus stops eating when her children are hatched. This does not occur if her optical glands are removed. Such an operation results in a four-fold increase in life span of the animal.52 Bamboo can live for 15–20 years reproducing vegetatively but then, in the year of flowering, dies at the height of the summer time immediately after the ripening of the seeds (see Skulachev8 for discussion). Striking observations were made in studies of salmon. The Pacific salmon was shown to die immediately after spawning as a result of accelerated aging (progeria), which develops when the fish leaves the ocean and swims along a river to its upper reaches. The traditional explanation of this kind of death was that the animal spends too much energy when swimming in the river for a long distance against current. However, this point of view proved to be wrong since (1) aging and death did not occur if gonads or adrenal glands were removed53 and (2) progeria was observed even when the river was very short and current was weak. In the Far East of Russia, two populations of salmon were compared, one spawning in the upper reaches of the Amur river (thousands of kilometers long) and another spawning in a very small river on the Sakhalin island (only 0.2 km long). In both cases, the spawning fish showed typical traits of aging that resulted in death. A signal for progeria proved to be change from the sea to fresh water. In this example, a biological function of suicide seems to be that the remains of the old fish become food for river invertebrates who, in turn, are food for the young fish.54
The Atlantic salmon, in contrast to its Pacific relative, after spawning in a river returns from river to ocean. If it is the summer generation of the fish, it often dies in the fall. A Russian ichthyologist V.V. Ziuganov has recently studied larvae of a mollusk (pearl mussel Margaritifera margaritifera) that develops in gills of the Atlantic salmon. He found that larvae can somehow switch off the fish’s “death program” so the larvae-infected fish live at least one season more than the majority of non-infected salmon (some of infected salmon live up to 13 years). An increase in the host’s life span is needed for the larvae to complete their own development. It was shown that the infected fish had fewer tumors and were more resistant to wounds and burns.54 Leng and colleagues55 reported that a peptide from another mollusk related to the mussel, a Mercenaria meretrix, activates superoxide dismutase but inhibits tyrosinase and proliferation of carcinoma cells. Earlier it was shown that a Mercenaria extract possesses anticancer activity and decreases the blood sugar and fat.55
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